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Chapter 15 : Vaccine Development

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Vaccine Development, Page 1 of 2

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Abstract:

This chapter reviews the history and recent attempts to develop a vaccine against HIV. Most experimental studies were conducted with SIV or SHIV strains in primates, particularly rhesus macaques, but other animal models have also been evaluated. By assessing past conventional vaccine approaches, a great deal has been learned about what procedures will not work. Now, new directions must be considered that are based on the knowledge that combating HIV infection requires recognition of virus-infected cells, not only free virions. This chapter talks about the true concept of vaccines—prevention of virus infection. Development of a vaccine for prevention of HIV infection has included approaches with inactivated virus, attenuated viruses, viral cores, and purified envelope gp120, alone or in association with live expression vectors (virus or bacteria). DNA inoculation offers a direction for a vaccine but has not recently given promising results. The ideal vaccine is one that is safe and long lasting. It will induce local immunity with cellular and humoral immune responses of both innate and adaptive type, as well as antibodies that neutralize and do not enhance the infection.

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15

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Figures

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Figure 15.1

The threshold hypothesis. After infection with a live attenuated virus, clinical outcomes can vary and depend on multifactorial host-virus dynamics. Persistently high viral loads exceeding the disease threshold result in fatal AIDS (pattern 1); due to high viral replication, more pathogenic viral variants inevitably emerge (pattern 1). If the viral burden exceeds a second putative threshold, the vaccine threshold, but remains below the disease threshold, the host will not develop disease but will instead generate protective responses against subsequent challenge with pathogenic virus (pattern 2, vaccine protection window). If the viral burden remains below the vaccine threshold, as in the case of highly attenuated virus variants, disease will not develop but the host will not be protected against subsequent virus challenge (patterns 3 and 4). If the viral load is so low that the seroconversion threshold is not reached, the host will only be transiently infected (pattern 4). During the chronic phase of infection, occasional blips of viremia can occur, perhaps due to transient disturbances of host control over the vaccine virus (patterns 5). However, live attenuated viruses persist and continue to replicate; with time, aggressive viral escape variants can emerge, causing disease at late stages (not shown). Due to genetic variability in outbred populations, host immune responses may vary considerably, making determination of a discrete vaccine protective window difficult. Adapted from reference 4746 with permission.

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Image of Figure 15.2
Figure 15.2

Stages in the entry, growth, movement, and spread of . The bacteria are en-docytosed, fused with intracellular vesicles, and digested, and their antigens can be expressed with class II molecules. Alternatively, they can replicate out of the vesicles, become digested, and subsequently be expressed with class I molecules. Because of the value in expressing antigens by these two processes, this bacterium is being evaluated for use in HIV vaccine development. From reference 4431, with permission.

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Image of Figure 15.3
Figure 15.3

Electron microscopy of virus-like particles (VLPs) forming in insect cells transfected with a baculovirus construct expressing Gag/Pol. (A) VLPs budding from the plasma membrane. (B) A high magnification showing several intermediate stages in the budding process. (C) Extracellular VLPs. Reprinted from reference 1933 with permission.

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Image of Figure 15.4
Figure 15.4

Interconnections of the mucosal immune system that involve the oral, nasal, urethral, vaginal, and rectal cavities. PP, Peyer’s patches. Provided by J. Mestecky.

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Image of Figure 15.5
Figure 15.5

Timeline for phase III vaccine trials held in Canada, Puerto Rico, The Netherlands, and the United States. Reprinted from reference 1350 with permission.

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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References

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Tables

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Table 15.1

Features of conventional vaccines

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.2

Possible correlates of protective immunity against HIV infection

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.3

Immunization approaches evaluated for an HIV vaccine

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.4

Potential animal models for developing an HIV vaccine

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.5

HIV vaccine approaches

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.6

Potential value of transgenic plants in vaccine development

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.7

Overall objectives of an AIDS vaccine

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.8

Challenges of developing an HIV vaccine

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.9

The ideal HIV vaccine

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.10

Vectors evaluated for HIV vaccines

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.11

Effective HIV immunization

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.12

Vaccination procedures involving the prime-boost approach

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.13

Important issues with DNA vaccines

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.14

Adjuvants to augment cell-mediated and humoral immune responses

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.15

What is the shortest time that an effective vaccine could be developed?

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.16

Factors involved in the completion of two phase III vaccine trials

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.17

Examples of presumed protection against HIV or SIV infection

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15
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Table 15.18

Development of licensed vaccines

Citation: Levy J. 2007. Vaccine Development, p 397-428. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch15

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